2006
DOI: 10.1113/jphysiol.2006.112250
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Potentiation of transient receptor potential V1 functions by the activation of metabotropic 5‐HT receptors in rat primary sensory neurons

Abstract: 5-Hydroxytryptamine (5-HT) is one of the major chemical mediators released in injured and

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Cited by 97 publications
(66 citation statements)
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References 65 publications
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“…Sensitization can arise from phosphorylation of TRPV1 at multiple sites via protein kinase C and protein kinase A downstream of activation of GTP-binding protein-coupling receptor by bradykinin, ATP, nerve growth factor, calcitonin gene-related peptide, and prostaglandins (10). Our recent report also showed that the metabotropic 5-HT receptor facilitates TRPV1 functions through protein kinase C/protein kinase A pathways (11). TRPV1 is subject to tonic inhibition by phosphatidylinositol 4,5-bisphosphate (PIP 2 ) (12), providing an additional biochemical pathway through which the activity of the channel can be regulated after GTPbinding protein-coupling receptor activation.…”
mentioning
confidence: 88%
“…Sensitization can arise from phosphorylation of TRPV1 at multiple sites via protein kinase C and protein kinase A downstream of activation of GTP-binding protein-coupling receptor by bradykinin, ATP, nerve growth factor, calcitonin gene-related peptide, and prostaglandins (10). Our recent report also showed that the metabotropic 5-HT receptor facilitates TRPV1 functions through protein kinase C/protein kinase A pathways (11). TRPV1 is subject to tonic inhibition by phosphatidylinositol 4,5-bisphosphate (PIP 2 ) (12), providing an additional biochemical pathway through which the activity of the channel can be regulated after GTPbinding protein-coupling receptor activation.…”
mentioning
confidence: 88%
“…Chemical mediators released from damaged tissue and inflammatory cells enhance the perception of pain by decreasing the activation threshold of transient receptor potential vanilloid 1 (TRPV1) through a variety of posttranslational mechanisms (Cesare and McNaughton, 1996;Khasar et al, 1999;Hu et al, 2002;Chuang et al, 2001;Ohta et al, 2006). Among these mechanisms, protein kinase A (PKA)-and PKC-mediated phosphorylation of serine residues is known to modulate the sensitivity of TRPV1 (Bhave et al, 2002;Numazaki et al, 2002).…”
Section: Introductionmentioning
confidence: 99%
“…5HT is released in injured and inflamed tissues and causes hyperalgesia. This potentiation is due to 5HT receptor-mediated activation of PKA and PKC (Ohta et al, 2006). NGF potentiates TRPV1 activation via binding to its TrkA receptor.…”
Section: Downloaded Frommentioning
confidence: 99%